Zoonotic Diseases of

Common Pet Birds:

Psittacine, Passerine, and
Columbiform Species
Erika E. Evans, DVM, MBA

KEYWORDS
• Pet • Bird • Zoonoses • Psittacine • Avian • Parrot
• Passerine • Columbiform

Psittacine, passerine, and columbiform birds are among the most popular groups of
avian species kept as pets. Fortunately, zoonotic transmission of disease from these
species is uncommon, but there are some recognized dangers. Most notably,
Chlamydophila psittaci can be transmitted from pet birds to humans. Salmonella spp,
although more commonly a food-borne zoonotic agent, can also be transmitted
through pet birds. Allergic responses to pet birds, including pneumonitis and contact
dermatitis, have also been documented. Bite wounds from pet birds are rarely
reported but can cause trauma and develop infection. The other diseases discussed
here are considered potential zoonotic diseases of pet birds because of either
isolated reports of suspected but unconfirmed transmission to humans or from
reports of wild conspecifics being reported to have the disease. For most diseases,
humans with underdeveloped or compromised immune systems, including the very
young, the elderly, HIV patients, individuals undergoing chemotherapy, or people
otherwise immunosuppressed due to other disease are the most at risk.

BACTERIAL ZOONOSES
Chlamydiosis
Chlamydiosis is a zoonotic disease of great interest to pet bird owners and has
received a vast amount of attention. Recently, the National Association of State Public
Health Veterinarians (NASPHV) has completed an updated compendium to assist in
the prevention and control of chlamydiosis among humans and pet birds.1 A free copy
of the compendium along with other resources to aid pet owners with infected birds,
pet stores, and aviaries working toward detection and prevention is available at the
NASPHV Web site.1

Avian and Zoological Medicine Service, Department of Small Animal Clinical Sciences, College of
Veterinary Medicine, University of Tennessee, 2407 River Drive, Knoxville, TN 37996, USA
E-mail address: rikievans@utk.edu

Vet Clin Exot Anim 14 (2011) 457-476

doi:10.1016/j.cvex.2011.05.001 vetexotic.theclinics.com
1094-9194/11/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
458 Evans

According to the Centers for Disease Control and Prevention, 66 human cases of
psittacosis were reported through the Nationally Notifiable Diseases Surveillance
System between 2005 and 20091; these statistics are likely an underrepresentation
due to incorrectly diagnosed or unreported cases.2 Most of the cases reported
between 2005 and 2009 were attributed to exposure to pet birds infected with the
bacterium.1 Cockatiels, parakeets, parrots, and macaws were the most commonly
represented species. Populations considered to be most at risk include bird owners,
pet shop employees, and veterinarians. Due to the zoonotic potential, C psittaci is
reportable in most states.
Chlamydiosis is caused by a small bacterial organism called C psittaci.2– 4 This
organism is a gram-negative, obligate intracellular bacterium that transitions through
at least 2 states during its life cycle. There is an elementary body stage that can infect
cells either within the same host or in another host, and a reticulate body stage, which
undergoes replication but is not able to infect other cells. An elementary body is
extracellular, highly infectious, and metabolically inactive. Elementary bodies are
resistant to many environmental stressors and can survive in soil for up to 3 months
and in bird droppings for up to 1 month. Elementary bodies are inhaled or ingested by
a host and attach themselves to an eukaryotic cell, most commonly a respiratory
epithelial cell. After attaching to the cell, the elementary body undergoes endocytosis
and forms an endocytoplasmic vesicle. This vesicle allows for the elementary body to
remain safe from the host’s immune defense system while it undergoes transition into
the reticulate body. The reticulate body is the intracellular, metabolically active state
that is capable of replication via binary fission. After replication, the reticulate bodies
convert to elementary bodies and are released from the cell. Depending on the strain,
host, and environmental conditions, the developmental cycle takes 48 to 72 hours.
There is also the possibility of a third persistent state in which the organism is present
and viable but cannot be eliminated by the host’s defense system.5– 6 If this state
exists, it is unlikely that a culture could successfully be obtained. The existence of this
persistent state is controversial and documentation of its existence in naturally
infected birds is lacking.
Birds infected with C psittaci may be asymptomatic.7,8(pp4 –96) This is especially
likely for pigeons and passerine birds, but is also seen with psittacine birds. Stress
due to reproduction, raising young, transportation, shipping, overcrowding, and
inadequate husbandry can increase the likelihood that birds will begin shedding the
organism and/or showing clinical signs. Immunosuppressed birds and very young
birds are most likely to succumb to severe infection. The organism can be transmitted
vertically, and the very young may die soon after hatching or while still in the nest.
The typical incubation period is anywhere from 3 days to several weeks, but
clinical signs and active disease may appear without any known risk or exposure.1
Many of the clinical signs seen in birds, such as lethargy, decreased appetite,
weight loss, and ruffled feathers, are very nonspecific. Disease of the respiratory,
gastrointestinal, and ocular systems may result in more visible clinical signs. Liver
disease due to C psittaci commonly results in lime-green diarrhea or bright green
urates. Conjunctivitis, dyspnea, and ocular and nasal discharge are often re-
ported. Severely affected birds may become completely anorexic, depressed, and
die. These clinical signs are not unique to chlamydiosis but may support a
potential diagnosis.
When a person becomes infected with C psittaci due to contact with a psittacine
bird, the disease process is called psittacosis and has historically been referred to as
parrot fever.9 If a person becomes infected with C psittaci as a result of contact with
a nonpsittacine bird, the term ornithosis is applied. Chlamydiosis is a broader term
 Zoonotic Diseases of Commonly Kept Pet Birds 459

that includes both psittacosis and ornithosis. All of these terms are used somewhat
interchangeably in publications regarding zoonoses.
Psittacosis occurs in multiple age groups, but the most severe manifestations of
infection are reported in people aged between 35 and 55 years.4 Children rarely show
severe signs when infected, and many individuals shown to be infected with the
bacterium show signs mild enough to require minimal to no treatment. The severity of
symptoms in people affected with C psittaci can range from subclinical to sepsis with
multiorgan failure. Many resources describe flulike symptoms such as fever, chills,
headache, muscle aches, and a dry cough as symptoms of human infection with C
psittaci. Headache is the most commonly reported sign, followed by cough, dyspnea,
confusion, and abnormal liver tests. Pneumonia diagnosed via thoracic radiographs is
also commonly reported. The vast majority of people infected with C psittaci show
mild signs, and when medical assistance is needed can be treated readily with
antibiotic therapy.
There are other less common, more severe expressions of the disease, such as
renal complications, hepatitis, pancreatitis, and reactive arthritis.4 Neurologic and
cardiac manifestations are also reported. Some infected individuals develop menin-
goencephalitis, with the most frequent clinical findings being fever, headache, and
confusion. Less commonly, status epilepticus, localized cerebellar ataxia, and brain-
stem encephalitis are also seen. Cardiac manifestations of the disease include
endocarditis, myocarditis, and pericarditis. Symptoms are often present for several
months prior to a diagnosis. Endocarditis can be complicated by the development of
glomerulonephritis, and surgery is often required even with appropriate and timely
antibiotic therapy. Surgical intervention for infective endocarditis is aimed at removing
infected tissue, draining any abscesses, repairing heart tissue damaged from the
infection, and repairing or replacing affected valves.10 Mortality with this syndrome
approaches 50%.4 Few other specific clinical presentations have been described in
humans, which fortunately are very infrequent, including a fulminant form of psitta-
cosis, gestational psittacosis, and chronic follicular meningitis.4
Psittaciforms, passeriforms, and columbiforms are among the 30 bird orders in which
C psittaci has been documented.11 Of these 3 orders of birds, most human cases are
associated with exposure to psittacine birds, but passerine birds and columbiform birds
are also recognized as sources of human infection.4 Risk of transmission increases with
close contact with infected birds that are actively shedding the organism. Birds under-
going stressful situations such as shipping, overcrowding, reproduction, or malnutrition
are more likely to shed, resulting in transmission.1 Birds that are shedding may not show
any sign of disease. Infection is acquired through inhalation of aerosolized organisms in
dried feces or respiratory tract secretions and through direct contact with infected birds.
Persons developing persistent flulike symptoms, headache, respiratory distress, fever,
confusion, or cough should consult with a physician and provide details regarding their
exposure and interaction with birds.4
A combination of tests, including culture, antibody detection, and antigen detec-
tion, are recommended when looking for evidence of infection with C psittaci infection
in birds.1 Infection can be difficult to detect, especially in asymptomatic birds. There
are no pathognomonic lesions that can be viewed on gross necropsy, but cloudy air
sacs and enlargement of the spleen and liver support a diagnosis of psittacosis.
Tissues or impression smears undergoing chromatic or immunologic staining can
sometimes aid in identifying organisms. Liver and spleen are preferred tissues for
bacterial culture.
In birds showing clinical signs, the use of a combined conjunctival, choanal, and
cloacal swab sample and/or liver biopsy can be used for bacteriologic culture or
460 Evans

Fig. 1. Sample collection for diagnostic tests, such as bacterial culture and PCR, often includes
swabbing the choana of a bird.

polymerase chain reaction (PCR; Fig. 1).1 Depending on the stage of infection and
affected tissue, birds may not shed detectable levels of the bacterium in their feces,
and for this reason the conjunctival and choanal swabs are preferred to feces. If feces
must be used, multiple collections of feces over 3 to 5 consecutive days should be
collected and submitted together as a single sample. Samples should be refrigerated
after collection and shipped on ice, but not frozen. The individual requirements of
each lab may differ, and the sampler is encouraged to contact individual laboratories
for their requirements since reliable detection of the bacterium relies heavily on
appropriate handling and processing of the samples.
Antibody tests are also available.1,12 Elementary-body agglutination detects IgM
antibody, an early indicator of infection, to the infectious from of C psittaci elementary
bodies. Indirect fluorescent antibody detects polyclonal secondary antibodies from
the host, primarily IgG. Complement fixation is a very sensitive test for antibody but
has been associated with a high rate of false-positives in parakeets, young African
greys, and lovebirds.1
A positive test may reflect either an active infection or an appropriate immunologic
response to a previous infection.12 Antibody might not be found in infected birds that
have been acutely infected and are not yet mounting a detectable immune response.
Antimicrobial treatment could result in undetectable antibodies, but IgG can persist
after successful treatment. To confirm a diagnosis of chlamydiosis, a positive
antibody titer must be paired with either 1) a second antibody titer showing at least a
fourfold or greater increase in titer, or 2) antigen identification.1 A positive antibody
titer with an elevated white blood cell count, increased serum liver enzymes, and
known exposure is not a definitive diagnosis, but are all highly suggestive of
chlamydiosis.
Antigen testing detects the presence of the organism even when it is not alive.1,11
Cross reacting antigens may result in false-positives, and false-negatives can occur
when the sample doesn’t contain sufficient antigen, which may be due to intermittent
shedding. Commercially available antigen tests include enzyme-linked immunosor-
bent assay and fluorescent antibody test. Positive antigen results should always be
 Zoonotic Diseases of Commonly Kept Pet Birds 461

evaluated with respect to the presence or absence of clinical signs in the bird. If the
bird is asymptomatic, verification that the bird is shedding the organism can be
pursued via isolation of the organism.
PCRs are available for testing on combined conjunctival, choanal, and cloacal
swab specimens or blood.1,13 PCR can be very sensitive and specific, but there are
no standardized PCR primers and techniques for handling, and processing samples
vary. A list of laboratories that currently offer testing for human and avian samples are
listed in the NASPHV’s compendium on avian chlamydiosis.1 PCR and culture for
avian samples are available at the Diagnostic Center for Population and Health at
Michigan State University (Lansing, MI, USA), the Infectious Diseases Laboratory at
the University of Georgia College of Veterinary Medicine (Athens, GA, USA), and
Texas Veterinary Medical Diagnostic Laboratory (College Station, TX, USA). Some of
these laboratories also offer antibody tests for avian samples. The Comparative
Pathology Laboratory at the University of Miami (Miami, FL, USA) offers enzyme-
linked immunosorbent assay, indirect fluorescent antibody, and PCR, whereas the
Diagnostic Virology Lab of the National Veterinary Services Laboratories (Ames, IA,
USA), offers culture and complement fixation. NASPHV recommends any birds that
are suspected to be infected with C psittaci be evaluated using more than 1 type of
test and that all tests are interpreted with regard to the bird’s history and clinical signs.
Some veterinarians suggest treating any birds that may be infected regardless of
test results, because of the zoonotic risk, but NASPHV discourages prophylactic
antibiotic treatment.1 Currently there is no documentation of antibiotic resistance to
C psittaci in birds, but antibiotic resistance has been reported to other Chlamydophila
species and is therefore of potential concern.14 Historically, the treatment of choice
was considered to be doxycycline administration for a minimum of 45 days in most
species and 30 days in budgerigars.1 Treatment for this length of time is still
recommended to avoid incomplete resolution of infection. However, recent studies
have indicated that other less lengthy protocols may be efficacious.15
Information regarding dosing and recipes for food and water administration to birds
are readily available in the compendium on avian chlamydiosis by NASPHV.1
Medicated food has successfully been used to treat chlamydiosis in budgerigars and
cockatiels.16,17 Suggested concentrations of doxycycline hyclate medicated water
are available for use in cockatiels, African grey parrots, and Goffin’s cockatoos.1
Exotic doves have also been successfully treated using doxycycline-medicated
water.18 Budgerigars do not maintain therapeutic concentrations using medicated
water and should be provided the medication via an alternative route. Some birds may
develop toxicosis in response to doxycycline. If toxicosis is suspected, treatment with
doxycycline should be discontinued and supportive care provided. Treatment can
later be attempted with either a reduced dose of doxycycline or alternative regimen.
Pharmacokinetic studies have been undertaken to determine if the use of other
medications or decreasing the length of administration of doxycycline from the
recommended 45 days may be effective. Oral administration of azithromycin given
every 48 hours or doxycycline given every 24 hours for a 21-day course of treatment
have both been shown to be effective in treating cockatiels experimentally infected
with C psittaci.15 These results have not yet been tested in naturally infected
cockatiels or any other bird species and therefore cannot yet replace the 45-day
recommended treatment. Primary motivation to reduce the required length of
treatment is to increase the likelihood of owner compliance and therefore decrease
recurrence of the disease.
Regardless of which treatment protocol is utilized, infected birds should be
isolated from other animals in clean, uncrowded cages.1 Appropriate husbandry
462 Evans

with adequate nutrition and clean water should be maintained to reduce the risk of
secondary infection. Birds should be weighed every 3 to 7 days, and if not able to
maintain their weight, supplemental and gavage feeding may be required. High
dietary intake of calcium from mineral blocks and cuttlebones should be avoided
since it can inhibit the absorption of oral tetracyclines. In hand-fed neonates that
require supplementation, calcium and tetracyclines should be given at least 4 to 6
hours apart. Facilities should be thoroughly cleaned and disinfected before termina-
tion of treatment to reduce the risk of reinfection. Two weeks after the completion of
treatment is the earliest suggested time period for repeat screening.
Birds that are sick should not be sold or purchased.1 Birds from multiple origins
should not be combined without proper quarantine (minimum 30 days) and multi-
modal testing (antibody, antigen, PCR) for the presence of C psittaci. Cages, food
containers, and water bowls should be positioned and cleaned to avoid the spread of
fecal matter, feather dander, contaminated food, and other substances between
cages. Fecal material and discharged food items should be removed daily. Prior to
removal, it is recommended that fecal material and contaminated cage items be
wetted or sprayed down to avoid aerosolization of the material. Ventilation should be
sufficient to avoid accumulation and limit spread of aerosolized organisms.
In multibird households or facilities, healthy birds should be cared for prior to
treatment and/or handling of infected birds.19 All debris and fecal material should be
scrubbed from cages. Disinfectants should be used to thoroughly clean any cages
that have housed infected birds before they are reused. Bleach and water at a 1:32
dilution (1/2 cup of 5% chlorine bleach in a gallon of water), 1% Lysol, and quaternary
ammonia compounds have been recommended as effective disinfectants. Most
disinfectants require at least 5 to 10 minutes of contact time and any items that
cannot be properly disinfected should be discarded. Rinse thoroughly to avoid
irritation from the detergent. Cleaning methods that limit the aerosolization of
materials, such as spraying down cages and floors prior to sweeping and mopping
should be used. Vacuum cleaners and pressure washers should be avoided because
of the risk of aerosolization.
Once clinical signs are noted in birds and a diagnosis of chlamydiosis obtained,
human contact and the potential for transmission has likely already occurred.
Therefore, any individuals caring for or surrounded by birds should be made aware of
the potential zoonotic risk. People cleaning cages or handling infected birds should
wear protective clothing that covers the hands, eyes, and head. These individuals
should be fitted with respirators of a N95 or higher rating. When potentially infected
birds are necropsied, the procedure should be completed in a biological safety
cabinet, and detergent and water should be used to avoid infectious particles
becoming aerosolized.

Salmonellosis
Another zoonotic bacterium with reported cases of suspected bird to human
transmission is Salmonella.20 There are 2 species of Salmonella with thousands of
different serovars.21,22 There are some serovars of Salmonella that are specifically
adapted for avian hosts, such as Salmonella Pullorum and Salmonella Gallinarum,
which primarily cause systemic disease in poultry.23 Certain strains of Salmonella
Typhimurium have been identified as being host adapted for causing disease in
pigeons.24 Salmonella infections with various serovars have been documented in
psittacine, passerine, and columbiform birds.25–27
Several factors will dictate the manifestation and severity of Salmonella infection in
pet birds.23,28 The ability of the bird to mount an effective immune response will
 Zoonotic Diseases of Commonly Kept Pet Birds 463

depend on the infecting serovar, age of the animal, and presence of concurrent
infection, malnutrition, poor husbandry, or stress, which may increase the risk of
severe and potentially fatal infection. Some serovars of Salmonella, such as S
Typhimurium or Salmonella Enteritidis are more likely to cause severe illness in both
birds and humans.
Salmonella has been shown to have the potential to infect multiple avian organs
of the respiratory, gastrointestinal, renal, neurologic, cardiovascular, and repro-
ductive systems.29(pp953– 6) Clinical signs reported in psittacine birds range from
mild enteritis to severe anorexia, diarrhea, lethargy, dehydration, and crop stasis
or sudden death. Salmonella spp have also been isolated from asymptomatic
birds. Suspected transmission of Salmonella Typhimurium from psittacine birds to
humans has been documented.9,30 –31
Pigeons infected with Salmonella spp may also show a wide variation in clinical
signs.26 Infected pigeons may be asymptomatic and therefore the introduction of new
birds, exposure to feral birds, or the routine racing and showing of pigeons carries risk
of exposure. In the United Kingdom, where pigeon racing and showing is common,
any isolates of Salmonella spp obtained from racing and show pigeons must be
reported to Animal Health due to zoonotic risk. Pigeons that have ingested the
bacterium may show signs of bacteremia and sepsis. Decreased appetite, weight
loss, and decreased egg production and viability are commonly seen. Some birds
may develop swollen and warm joints from septic or infectious arthritis or exhibit
evidence of central nervous system disease.
Wild passerines, both ill and asymptomatic, have been repeatedly documented as
carriers of Salmonella spp and have been implicated in the transmission of the
bacterium to mammals and to humans.32,33 As seen with infection in other avian
species, Salmonella Typhimurium in passerines may manifest as systemic and
multiorgan disease.29(pp953– 6) Granulomas have been observed in the liver, spleen,
and ceca. Finches and canaries, 2 of the most popular passerines species kept as
pets in the United States, have also been shown to exhibit ocular lesions and
osteomyelitis.34
Salmonellosis in people is usually the result of food borne illness or direct contact
with an infected reptile or amphibian, rather than interaction with a pet bird.35,36 Some
individuals that ingest Salmonella spp may have no to mild signs of illness.37 Most
individuals that become ill from ingesting Salmonella spp have symptoms for 4 to 7
days. Clinical symptoms include abdominal cramps, headache, fever, nausea,
vomiting, and copious watery diarrhea. Occasionally the symptoms may be severe
enough that hospitalization in indicated. Rarely, serious complication or death may
result from infection. In addition to causing gastrointestinal distress, some patients
experience other systemic manifestations of infection with the bacterium, including,
but not limited to, arthritis, hepatitis, and neuritis. The very young, the elderly, and
people with underlying health issues are most likely to suffer severe disease.
The bacterium is typically spread via fecal to oral transmission but can also be
spread through direct contact with infected animals or people.35 The bacteria may be
spread mechanically via contaminated clothing, shoes, equipment, and on rodents
such as rats and mice.26 This disease can also be transmitted vertically into the egg
or through crop milk. Food and water contaminated with feces from infected animals,
both wild and domestic, is also a potential source of infection.
Definitive diagnosis of salmonellosis requires successful culture of the organism.
Antemortem, repeat, or pooled fecal samples are cultured. The use of selective
enriched culture media is required, and laboratories must be told that salmonellosis
is suspected. The shedding of the bacterium is often intermittent and false-negatives
464 Evans

are common. Postmortem, multiple samples from a wide range of tissues should be
submitted for culture. In flocks with large die off, multiple birds should be submitted
for evaluation.
The severity of the disease presentation dictates the intensity of treatment.26
Supportive care, including fluids and gavage feeding, may be indicated. Antibiotic
use is controversial because resistance is common; if warranted, antibiotic choice
is best determined by the result of culture and susceptibility testing. Enrofloxacin
and amoxicillin are common choices. Maintaining cleanliness within the cages or
lofts and providing clean water and food are essential in allowing for recovery.
Length of treatment may last from 10 days to 3 weeks to allow for clearance of the
bacteria.
Prevention of Salmonella spp infection relies heavily on cleanliness.37 Appropriate
husbandry must be maintained, providing for clean surroundings, clean food and
water, and avoiding contact with ill and infected animals. Any materials with infected
feces should be removed from the enclosure. Sodium hypochlorite (bleach) at a
concentration of 0.05% and alkaline peroxide at a concentration of 1% have been
shown to be effective against Salmonella.38 The effectiveness of some disinfectants
against Salmonella adhered to surfaces or contained within a biofilm may be
reduced.39 Suggestions for disinfectants to combat Salmonella in these situations
include those containing 70% ethanol. Virkon S was also effective at eliminating
Salmonella found on surfaces. Rodent control should be implemented.26 Humans
working with animals that may carry Salmonella spp should wear disposable gloves,
frequently wash their hands, discard any items sullied with feces, and avoid eating,
drinking, or putting hands near the face and mouth without appropriately washing
with soap and warm water.37

Mycobacteriosis
Mycobacterium spp are Gram positive, aerobic, acid-fast bacillus that infect birds,
mammals, and humans.40 The most commonly isolated Mycobacterium spp from pet
birds are Mycobacterium avium and Mycobacterium genevense. Other species of
Mycobacterium are infrequently identified in pet birds, including Mycobacterium
tuberculosis, the agent responsible for tuberculosis in people. M avium subsp
Hominis suis has also been diagnosed in a 6-month-old female, blue-fronted Amazon
parrot with inappetence, slight emaciation, heavy biliverdinuria, ascites, and me-
lena.41 This subspecies rarely causes disease in birds, but has been shown to cause
severe disease in humans, especially immunocompromised individuals.
Clinical signs of mycobacteriosis in birds vary widely dependent on the
Mycobacterium spp, resulting in infection, the species of bird affected, the
duration and severity of exposure, and the organ system infected.41 Weight loss
is the most consistent finding reported across multiple species. Respiratory
disease can occur, but diarrhea, coelomic distension, and poor feathering are
more frequently reported.42 Weight loss and failure to respond to routine antibiotic
therapy are commonly documented in pet birds shown to be suffering from
mycobacteriosis.
People afflicted with acquired immune deficiency syndrome are commonly afflicted
with what is known as the Mycobacterium complex (M avium and Mycobacterium
intracellulare) and are the individuals most likely to develop systemic mycobacterio-
sis.40,43– 44 The likelihood of infection increases directly with the severity of immuno-
suppression. Individuals undergoing organ transplant or those experiencing disease
resulting in immunosuppression are also at risk. Fever, weight loss, abdominal pain,
fatigue, chronic diarrhea, and anemia are reported in people with systemic mycobacteriosis.
 Zoonotic Diseases of Commonly Kept Pet Birds 465

Localized disease also occurs in humans including central nervous system infection,
boney or soft tissue lesions, cervical lymphadenitis, or endocarditis.43
M tuberculosis causes pulmonary disease known as tuberculosis in humans
characterized by a persistent cough, chest pain, and coughing up blood and/or
sputum.45 Other signs include weight loss, fatigue, fever, and generalized malaise.
Other parts of the human body may also be impacted by this infection including the
kidneys, spine, and brain. Tuberculosis was once the leading cause of death in the
United States and is still a common fatal illness in other parts of the world. Many
individuals who become infected with M tuberculosis develop latent infection be-
cause their immune systems are able to fight the disease. Latent infections can
transition to active infection within the body, causing illness when a person’s immune
system is not able to fight the infection. Infection can stay latent weeks to several
years, and those with suppressed immune systems, such as those with acquired
immunodeficiency system, are at increased risk of becoming ill.
Mycobacterium spp are very stable in the environment and can remain in the soil
for years.40 Infection is typically secondary to ingestion of the bacterium, inhalation of
the organism, or from introduction of the organism into open cutaneous lesions.
Mycobacterium organisms are found worldwide and have been isolated from soil,
water, animals, birds, and foods. Environmental sources such as contaminated water,
food, and soil are considered the most likely sources of infection for people and
animals. Possible transmission of M tuberculosis from humans to pet birds, including
an African grey and a green-winged macaw, has been reported, and there is concern
that a pet bird could harbor this organism and serve as a carrier and source of
infection to other birds and humans.46,47 M tuberculosis has also been identified in
pet passerines.48 No confirmed transmission of Mycobacterium from a bird to a
person has been reported.
Characteristic hemogram findings for birds diagnosed with mycobacteriosis in-
clude nonregenerative anemia, and leukocytosis with heterophilia and monocytosis.40
Depending on the organs most affected, lesions may include pulmonary granulomas,
enlarged liver, engorged intestinal loops, or boney lesions. A presumptive diagnosis
of mycobacteriosis may be made if acid-fast bacilli are detected in biopsy or necropsy
specimens. However, mycobacterial culture or polymerase chain reaction analysis is
required for definitive diagnosis. Care must be taken when acid-fast organisms are
detected in fecal samples, as nonpathogenic acid-fast organisms, including sapro-
phytes, may be present. Due to the prolonged period of time often necessary to
culture Mycobacterium spp, diagnosis in birds is often based on histological evidence
of mycobacteriosis in diseased tissue (liver, spleen, intestine) and PCR.49
Therapy is controversial due to the potential for persistent infection, antibiotic
resistance, and the zoonotic potential.40 If owners want to pursue therapy for a pet
bird, it is recommended that the veterinarian have owners sign a release that explains
the possibility of transmission of Mycobacterium from the bird.50 Successful treat-
ment has been achieved in pet birds with multimodal antibiotic therapy.40 Several
protocols are available with most, including drugs such as clarithromycin or azithro-
mycin, rifampin or rifabutin, and ethambutol. Treatment takes many months, and
monitoring success of treatment is difficult as the organism can be difficult to detect
in low numbers.
Reports of transmission of Mycobacterium spp to humans from pet birds is lacking.
However, there is a recognized potential for human transmission with pet birds
potentially serving as reservoirs. Prevention of mycobacteriosis relies heavily on
prompt detection of the bacterium and avoiding humans and birds that are showing
signs of illness. Maintaining overall health through proper diet and exercise supports
466 Evans

a healthy immune system that reduces risk of infection. Making sure that food, water,
and the environment are free of contamination can aide in prevention. Mycobacterium
spp can be challenging to destroy and are often resistant to commonly used
disinfectants.51 Bleach, one of the most commonly used disinfectants is only effective
at high concentrations and quaternary ammoniums are not effective. Phenolics are
the best disinfectant for inactivating M tuberculosis and potentially other Mycobac-
terium spp. Care must be taken to avoid generating droplets or aerosols when
cleaning, as inhalation is a primary means of transmission. If a person believes that
they or their bird have been exposed to individuals infected with Mycobacterium spp
they should seek medical or veterinary attention respectively.

Other Bacteria
There are multiple other potential bacterial zoonotic pathogens, including Myco-
plasma, a bacterium characterized by the lack of a cell wall, which causes conjunc-
tivitis, tracheitis, air sacculitis, and chronic respiratory disease most commonly in
poultry and wild passerines, but also in pet birds.52 Multiple gram-negative bacteria
such as Pasteurella spp, Klebsiella spp, Yersinia spp, Campylobacteriosis spp, and
Escherichia coli are also potential zoonotic pathogens identified in pet birds. Docu-
mented evidence of zoonotic transmission to humans from pet birds is lacking for
these bacterial pathogens but the potential is present. Appropriate hygiene and
husbandry, quarantine of sick birds, and maintaining clean food and water sources
will reduce risk of infection and possible transmission.

Viral Zoonoses
Avian paramyxovirus, avian influenza, and West Nile virus (WNV) are potential
zoonotic infectious agents found in pet bird species. There are not currently any
documented cases of direct transmission of these viruses from pet birds to humans,
but pet birds have the potential to serve as reservoirs for viral infection. Poultry and
wild bird populations, which are discussed elsewhere in this publication, are more
likely to harbor these viruses, and therefore, discussion of these viruses within this
chapter on pet birds will be abbreviated.

Newcastle Disease Virus

Avian paramyxoviruses (APMV) have been observed in pet birds, but most published
descriptions of APMV are based on poultry. APMV includes Newcastle disease virus
(NDV), which is caused by serotype 1 (APMV-1).53 There are nine serovars of avian
paramyxovirus, and each serotype is characterized by the type of bird affected.
PMV-1 is of great concern in the poultry industry and is a potential zoonotic disease.
In humans, NDV infection may result in mild flulike symptoms, conjunctivitis, or
laryngitis. Classic Newcastle disease was observed to infect pigeons during poultry
outbreaks in the United Kingdom.26 There is documentation that imported psittacine
birds may carry APMV, and passerines have also been shown to suffer from avian
paramyxovirus.54 –56 Pigeons may become infected with a variant strain similar— but
distinct from—the classic NDV, which is often referred to as PMV-1 or PPMV-1.26
Monoclonal antibodies are utilized to differentiate this strain from classic exotic
Newcastle disease. Vaccination of pigeons for PMV-1 is now a requirement for show
and racing pigeons in the United Kingdom.
The virus is shed through respiratory secretions and feces, and exposure to NDV is
usually due to ingestion or inhalation of contaminated substances.53 Direct transmis-
sion is possible, and vectors such as insects, humans, and rodents can exacerbate
 Zoonotic Diseases of Commonly Kept Pet Birds 467

the extent of infection. To confirm a diagnosis, isolation of the virus from infected
tissues to identify serotype and virulence must be completed. Antemortem samples
typically include cloacal and tracheal swabs. In birds, treatment is supportive and
most cases are fatal. Prevention through use of personal protective equipment and
good husbandry practices is encouraged to avoid infection.

Influenza
Avian influenza or influenza A is in the family Orthomyxoviridae and has been
associated with respiratory disease in multiple avian species, mammals, and hu-
mans.57 There is great variance in clinical signs dependent on the strain and
associated virulence and the susceptibility of the infected species.58 The virus is
classified according to surface proteins called hemagglutinin (H) and neuraminidase
(N); there are 16 H and 9 N unique proteins currently identified. Many wild birds,
especially waterfowl, infected with the virus are asymptomatic and serve as a
reservoir for a strain that may result in disease in domestic birds. A highly pathogenic
strain, H5N1, has caused significant poultry losses and human disease and death
predominantly in Asia over the past decade. This virulent strain also caused death in
birds that are typically reservoirs for the virus, including free-ranging ducks, shore-
birds, and passerines.59
Mild to severe respiratory signs are often accompanied by depression, anorexia,
diarrhea, or neurologic signs in birds.58 Inhalation or direct contact with respiratory,
fecal, or ocular secretions are the main modes of transmission.58,59 Antemortem
diagnosis is conducted via viral isolation from tracheal and/or cloacal swabs.58
Vaccinations are available for birds and have been used in an effort to protect some
valuable zoological species of birds; however, due to the potential zoonotic and
economic impact, there are strict legal restrictions governing their use.60 Potential
disadvantages of the use of the vaccine include the masking of clinical signs of
infection, which could translate into human exposure and possible infection.
There are no current reports of H5N1 in pet birds within the United States; however,
there is a report of low pathogenic H5N2 isolated from a 3-month-old red-lored
Amazon parrot with severe lethargy and gastrointestinal distress, including regurgi-
tation and melena.61 The bird was kept in quarantine, given supportive care, and
recovered from clinical signs within 4 days. The bird was released 9 weeks after
presentation when virus isolation and PCR were negative for the previously identified
virus. Avian influenza subtypes H5 and H7 are reportable in the United States, and
most often result in depopulation within the poultry industry due to the risk of the virus
mutating into a highly pathogenic form. However, as demonstrated in the aforemen-
tioned case, not all pet birds are destroyed.
Precautions recommended by the US Department of Agriculture can be taken to
protect pet birds from acquiring infectious diseases such as Newcastle disease and
avian influenza.62 First, owners should limit access to their pets. Allowing contact with
individuals whom own their own birds, have exposure to sick birds, or work in
occupations dealing with birds such as pet stores or poultry plants should be avoided.
Owners should make sure their hands and clothes are clean prior to handling their
pets. Food and water should be replaced daily. Cages should be kept clean and
droppings removed from any toys or materials kept within the household prior to
disinfection. If acquiring a new pet bird, proof that the bird was legally imported or
bred within the United States should be requested from the seller. Sick birds should
never be purchased and new birds should be quarantined for at least 30 days. If a pet
bird has been to a show, club meeting, or other event involving exposure to multiple
birds, that pet should be kept separate from any other birds in the household for at
468 Evans

least 2 weeks. Any birds showing signs of illness should be examined, and multiple
deaths within a pet bird collection should be reported to the U.S. Department of
Agriculture.

WNV
WNV is a flavivirus for which wild birds have been identified as the main reservoir.63
The virus causes neurologic and ocular disease in birds and has been associated with
neurologic and respiratory manifestations in mammals including humans. The virus
was first identified in 1999 in the Western Hemisphere, where wild and zoo birds in the
New York City area started dying from the virus. Species commonly kept as pets,
including passerine and psittacine birds, have been fatally infected with WNV and may
serve as a potential reservoir for human infection.64,65
Mosquitoes, primarily Culex spp, are the primary route of transmission.63,64,66 The
mosquito becomes infected when feeding on birds infected with the virus and then
spreads the virus to mammals, including humans, when the mosquito bites. Oral
transmission of the virus through ingestion of infected food items or from direct bird
to bird contact as occurs in courtship behavior has been reported. Direct contact,
organ transplant, intrauterine contact, and receiving blood donation products have
been documented as transmission routes in human infections.
Infected birds often display varying degrees of neurologic compromise, including
recumbency and paralysis of the pelvic and thoracic limbs. Virus isolation is best
achieved from the brain, spleen, and kidneys. PCR is available and typically
performed on oral or cloacal swabs, but is not always successful in antemortem
diagnosis.
Clinical symptoms in humans develop 3 to 14 days after being bitten by an infected
mosquito. Approximately 80% of people infected with WNV will show no symp-
toms.67 Up to 20% of people will show mild signs including fever, headache, nausea,
vomiting, and rash. Clinical signs can last for days to weeks. Rarely severe clinical
signs such as high fever, neck stiffness, disorientation, tremors, convulsions, weak-
ness, vision loss, numbness, and paralysis may occur. The duration of illness may last
weeks and neurologic detriments may be permanent.
Treatment for infection with WNV is primarily supportive. There is no specific
treatment, and in birds, infection severe enough to result in neurologic impairment is
often fatal. Minor clinical signs identified in people such as fever and muscle aches
may pass without any therapy. Severe cases of infection in humans will require
hospitalization, intravenous fluid therapy, breathing assistance, and additional sup-
portive care.
Limiting exposure to mosquitoes is the primary goal in prevention. Standing water
and areas that promote insect breeding should be treated with larvicides. People
should wear repellents when outdoors. Poultry houses and other avian enclosures,
including aviaries for zoological species and pet birds, should be constructed to limit
insect exposure. Many facilities within the United States that keep captive avian
species have started vaccination programs using a commercially available equine
vaccine, but efficacy is unknown.58 Due to concerns over safety and efficacy,
vaccination for WNV is not routinely done for pet birds but may be considered in pet
birds kept outside with exposure to wild birds and mosquitoes.

Fungal Zoonoses
There are multiple fungal organisms that can infect both birds and humans.68
Aspergillus spp and Candida spp are frequently responsible for respiratory or
gastrointestinal illness in pet birds, respectively, and can also result in severe disease
 Zoonotic Diseases of Commonly Kept Pet Birds 469

in immunocompromised individuals. There is currently no evidence that humans

acquire these fungal infections directly from birds, but rather acquire infections from
environmental exposure.
Some fungal organisms, including Cryptococcus spp and Histoplasmosis spp,
grow well in soil with high nitrogen levels, which is often due to the presence of bird
and/or bat feces. Histoplasmosis capsulatum is most commonly associated with dove
and pigeon feces, and the avoidance of areas that contain high levels of bird and bat
droppings are recommended. In most cases, infection with these organisms goes
unnoticed and humans are asymptomatic. In a few cases, symptoms of respiratory
disease, including cough, headache, chest pain, and fever, can result. In rare cases,
histoplasmosis can become disseminated and spread to organs outside the lungs.
Cryptococcus neoformans has a tendency to infect the central nervous system and
can result in meningoencephalitis. When symptoms are severe or the person is
immunocompromised, infection without appropriate antifungal treatment can be fatal.
Birds rarely develop clinical signs associated with colonization of C neoformans.
There is one report of a Moluccan cockatoo suffering from systemic cryptococcal
disease and one report of a cockatoo that exhibited cutaneous lesions.69,70 Human
infection with these organisms is not from direct transmission from a bird, but rather
from exposure to the organisms in the environment, and therefore—strictly speak-
ing—is not considered zoonotic. However, some of these fungal organisms may be
found in the feces of caged birds and therefore, pet birds may serve as a potential
reservoir for infection.71–75 Individuals who are immunocompromised are considered
at risk, and rarely, otherwise healthy individuals may become ill from infection with
Cryptococcus spp.76
There are 2 reports of meningitis from C neoformans in the literature that are
believed to be due to exposure to a pet bird’s contaminated and aerosolized excreta.
An elderly, immunocompromised woman was diagnosed with meningitis from an
isolate of C neoformans identical to one recovered from the feces of an asymptomatic
Umbrella cockatoo cared for in the same household.77 Exposure to aerosolized
cockatoo excreta containing C neoformans was cited as the suspected cause of
human infection. Although the bird had shared the same home with the woman for 7
years, the bird was housed on a different floor of the house and the woman was not
directly involved in caring for the bird or cleaning its cage. In the second case, an
immunocompetent woman was diagnosed with Cryptococcus meningitis after expo-
sure to a magpie bird kept as a pet in her parent’s household.78 The magpie’s feces
cultured positive for C neoformans. No direct contact with the bird was identified and
the woman had only lived in the house with the bird for 3 months. Consistent with the
suspected aerosol exposure described in these cases, experimentally, C neoformans
has successfully been isolated from air near caged birds.79 Cutaneous nodular
lesions due to dermatologic infection with Cryptococcosis spp have also been
observed in an immunocompromised pet cockatoo owner, but the origin of the
infection was not published.80

Parasitic Zoonoses
Species of birds kept as pets have been diagnosed with Giardia spp and Cryptospo-
ridium spp.81– 83 However, to the author’s knowledge there are no reports of direct
transmission from a pet bird to a human in the literature. There are reports of wild
birds serving as possible reservoirs for the parasites, increasing the possibility of pet
birds also serving as reservoirs.84 – 89
Most Giardia spp isolated from birds, such as Giardia ardeae and Giardia psittaci
are not considered zoonotic due to their host specificity.81 However, 1 species
470 Evans

isolated from psittacine birds, Giardia duodenalis may be infectious to humans. G

duodenalis trophozoites isolated from a parrot (Cacatua galerita) were used to
colonize the small intestinal tracts of domestic kittens and lambs.90 The experimental
infection resulted in diarrhea in most of the kittens, but the lambs remained
asymptomatic. This indicates that this Giardia sp may infect some pet bird species,
resulting in a potential source of infection and disease for some mammals, potentially
including humans.
Cryptosporidium spp reside in the gastrointestinal system of infected humans and
animals.91 The organism can be passed in droppings, and contaminated water is the
most frequently cited source of infection. Research indicates that wild birds including
songbirds, parrots, and pigeons may be a mechanical vector for this parasite,
increasing the risk of pet bird and human exposure.75,81– 83
Ectoparasites found on birds have the potential to cause dermatologic lesions in
humans.20 Mites, including Ornithonyssus sylviarum and Dermanyssus gallinae, most
commonly infect poultry and wild birds and are very rare in pet birds.92 Human skin
serves as an incidental host and lesions are mostly localized, but can be intensely
pruritic. Papular to papulovesicular eruptions in response to the mite can also occur.
These mites cannot reproduce on a human host and thus, the infection is self-limiting.
The sections of this publication focusing on zoonotic infections from poultry and wild
bird populations should be consulted for additional information.

Hypersensitivities and Dermatologic Conditions

Hypersensitivity pneumonitis (HP) is a lung disease characterized by lymphocytic
inflammation and formation of granulomatous pulmonary lesions resulting from an
inhaled antigen.93 Dust and mites encountered during occupational exposure have
historically been the most frequently cited antigens, however case reports of HP
resulting from exposure to pet birds, including psittacine and columbiform species,
are increasing in frequency. Exposure to feathers, feather dander, and bird droppings
have all been linked to allergic alveolitis. In addition to pet bird exposure, bedding
filled with feathers from species of waterfowl and poultry has also been implicated in
causing HP.
There are documented reports of pet birds suffering from a suspected similar
allergic pneumonitis.94 Most instances involve South American psittacine birds
exposed to the feather dander in the environment from another avian species, most
notably cockatoos and cockatiels. This disease is commonly called chronic obstruc-
tive pulmonary disease or macaw pulmonary hypersensitivity because of the over-
representation of blue and gold macaws (Ara ararauna).95 Although early stages of the
disorder often go unnoticed, advanced stages are often characterized by polycythe-
mia and exercise intolerance.96 Atrial smooth muscle hypertrophy is the most
prominent lesion, but proliferation of parabronchial lymphoid tissue and lymphoid
nodular formation may also occur. Treatment is based on symptomatic therapy, air
purification, and removal of the inciting antigen.
In people, HP can present as either an acute or chronic form.93,97 The acute form
often results in symptoms 4 to 6 hours after exposure to the antigen. Cough, fever,
chest pain, dyspnea, and generalized malaise are common symptoms of acute
exposure to an antigen to which the individual has hypersensitivity. In the chronic
form, signs are more gradual, but often progressive and can include breathlessness
that is exacerbated during exercise, a dry cough, decreased appetite, and unplanned
weight loss. There may be a genetic predisposition in people that results in the
development of HP.93 Diagnosis is often based on history of antigen exposure, clinical
symptoms, blood work, and imaging (including chest radiographs and CT). In some
 Zoonotic Diseases of Commonly Kept Pet Birds 471

cases bronchoscopy with biopsies, pulmonary function tests, and antibody panels to
detect specific hypersensitivities may also be performed. Treatment involves identi-
fying and avoiding the antigen, which can be difficult when the bird is living in the
home as a pet. Removal of carpeting, regular cleaning, and air filtration can reduce
antigen burdens in the home. For individuals breeding birds, a change in occupation
may be necessary. Glucocorticoids may be given to reduce inflammation in the
chronic form of the disease. When exposure to the antigen continues and treatment
is not initiated, irreversible pulmonary fibrosis and/or emphysema may result.
Birds most commonly reported to be associated with the development of HP
include pigeons and budgerigars.98 It is possible that this overrepresentation may be
due to the popularity of these species as pets. Other avian species frequently cared
for as pets, including canaries and various other psittacine birds such as cockatiels,
lovebirds, and rosella parrots have also been associated with HP in humans.99,100
Cutaneous reactions from skin allergies can also result from dermatologic expo-
sure to pet birds.101 Additionally, as most pet bird owners know, pet birds can bite
and cause significant skin lesions. Despite the fact that animal bites are the most
commonly documented zoonotic risk from pets, bites and scratches from pet birds
are rarely reported in peer-reviewed literature. However, secondary infection devel-
oped following a bite from a pet cockatoo in a 68-year-old woman.102 She was bitten
on her right hand between the second and third digits; the woman did not seek
professional medical advice until 30 days after the bite occurred. Culture of the lesion
was positive for Mycobacterium chelonae/abscessus. The wound was surgically
excised and long-term antibiotic therapy for 12 months was eventually successful. A
second report documents a 59-year-old diabetic woman who was diagnosed with
pyoderma gangrenosum after being bitten and scratched by a crow.103 Pyoderma
gangrenosum, a rare noninfectious neutrophilic dermatosis is typically associated
with an underlying systemic disease. The initial bite wound cultured positive for
Citrobacter koseri and E coli, both of which have been cultured from the gastrointes-
tinal tract of birds. Although bird bite reports are rare in the literature, the potential for
severe tissue damage, infection, and systemic illness exist, and those suffering bites
from pet birds should perform appropriate wound care, including cleaning and
flushing, and seek medical attention when appropriate. Research is needed to more
fully assess the risk associated with bites sustained from pet birds, particularly
infection that can occur due to inoculation of bacteria into the wound.
SUMMARY

In summary, true zoonotic infection resulting from exposure to pet birds is rare. Most
birds with potentially zoonotic diseases do not present serious risk to healthy individuals,
but all individuals interacting with birds should observe proper hygiene practices to lessen
the risk of transmission. Individuals handling pet birds or their excretions should ensure
proper sanitation. Veterinarians play multiple critical roles in limiting exposure to zoonotic
and potentially zoonotic diseases. Routine and preventative veterinary care can aid in the
recognition and treatment of disease. By developing a thorough understanding of the
diseases and methods of transmission, veterinarians can effectively communicate risks
and appropriate precautions to their staff and pet bird owners.
REFERENCES

1. Smith KA, Campbell CT, Murphy J, et al. Compendium of measures to control

Chlamydophila psittaci infection among humans (psittacosis) and pet birds (avian
chlamydiosis). Available at: http://www.nasphv.org/Documents/Psittacosis.pdf. Ac-
cessed February 10, 2011.
472 Evans

2. Centers for Disease Control and Prevention. Psittacosis. Available at: http://www.
cdc.gov/ncidod/dbmd/diseaseinfo/psittacosis_t.htm. Accessed February 10, 2011.
3. Vanrompay D, Ducatelle R, Haesebrouck F. Chlamydia psittaci infections: a review
with emphasis on avian chlamydiosis. Vet Microbiol 1995;45(2–3):93–119.
4. Stewardson AJ, Grayson ML. Psittacosis. Infect Dis Clin North Am 2010;24(1):7–25.
5. Hogan RJ, Mathews SA, Mukhopadhyay S, et al. Chlamydial persistence: beyond
the biphasic paradigm. Infect Immun 2004;72(4):1843–55.
6. Beatty WL, Morrison RP, Byrne GI. Persistent chlamydiae: from cell culture to a
paradigm for chlamydial pathogenesis. Microbiol Rev 1994;58(4):686 –99.
7. Flammer K. Chlamydia. In: Altman RB, Clubb SL, Dorrestein GM, et al, editors. Avian
medicine and surgery. Philadelphia: WB Saunders Co; 1997:364 –79.
8. Gerlach H. Chlamydia. In: Ritchie BW, Harrison GJ, Harrison LR, editors. Avian
medicine: principles and application. Lake Worth (FL): Wingers Publishing, Inc; 1994.
9. Grimes JE. Zoonoses acquired from pet birds. Vet Clin North Am Small Anim Pract
1987;17(1):209 –18.
10. Olaison L, Pettersson G. Current best practices and guidelines. Indications for
surgical intervention in infective endocarditis. Cardiol Clin 2003;21(2):235–51.
11. Kaleta EF, Taday EMA. Avian host range of Chlamydophila spp. based on isolation,
antigen detection and serology. Avian Pathol 2003;32(5):435– 62.
12. Grimes JE, Arizmendi F, Carter CN, et al. Diagnostic serologic testing of cage and
aviary birds for chlamydiosis and suggested confirmatory testing. J Vet Diagn Invest
1996;8(1):38 – 44.
13. Geens T, Dewitte A, Boon N, et al. Development of a Chlamydophila psittaci
species-specific and genotype-specific real-time PCR. Vet Res 2005;36(5– 6):
787–97.
14. Dugan J, Rockey DD, Jones L, et al. Tetracycline resistance in Chlamydia suis
mediated by genomic islands inserted into the chlamydial inv-like gene. Antimicrob
Agents Chemother 2004;48(10):3989 –95.
15. Guzman DS, Diaz-Figueroa O, Tully T Jr, et al. Evaluating 21-day doxycycline and
azithromycin treatments for experimental Chlamydophila psittaci infection in cocka-
tiels (Nymphicus hollandicus). J Avian Med Surg 2010;24(1):35– 45.
16. Flammer K, Trogdon MM, Papich M. Assessment of plasma concentrations of
doxycycline in budgerigars fed medicated seed or water. J Am Vet Med Assoc
2003;223(7):993– 8.
17. Powers LV, Flammer K, Papich M. Preliminary investigation of doxycycline plasma
concentrations in cockatiels (Nymphicus hollandicus) after administration by injec-
tion or in water or feed. J Avian Med Surg 2000;14(1):23–30.
18. Padilla LR, Flammer K, Miller RE. Doxycycline-medicated drinking water for
treatment of Chlamydophila psittaci in exotic doves. J Avian Med Surg 2005;
19(2):88 –91.
19. National Association of State Public Health Veterinarians. Psittacosis and avian
chlamydiosis checklist for owners of infected birds. Available at: http://www.nasphv.
org/Documents/PsittacosisChecklistOwners.pdf. Accessed February 10, 2011.
20. Jorn KS, Thompson KM, Larson JM, et al. Polly can make you sick: pet bird-
associated diseases. Cleve Clin J Med 2009;76(4):235– 43.
21. Brenner FW, Villar RG, Angulo FJ, et al. Salmonella nomenclature. J Clin Microbiol
2000;38(7):2465–7.
22. Heyndrickx M, Pasmans F, Ducatelle R, et al. Recent changes in Salmonella
nomenclature: the need for clarification. Vet J 2005;170(3):275–7.
 Zoonotic Diseases of Commonly Kept Pet Birds 473

23. Lister SA, Barrow P. Enterobacteriaceae. In: Pattison M, McMullin PF, Bradbury JM,
et al, editors. Poultry diseases. 6th edition. Edinburgh (Scotland): Saunders Elsevier;
2008. p. 110 – 45.
24. Pasmans F, Van Immerseel F, Heyndrickx M, et al. Host adaptation of pigeon isolates
of Salmonella enterica subsp. enterica serovar Typhimurium variant Copenhagen
phage type 99 is associated with enhanced macrophage cytotoxicity. Infect Immun
2003;71(10):6068 –74.
25. Vigo GB, Origlia J, Gornatti D, et al. Isolation of Salmonella typhimurium from dead
blue and gold macaws (Ara ararauna). Avian Dis 2009;53(1):135– 8.
26. Pennycott T. Pigeons: infectious diseases. In: Chitty J, Lierz M, editors. BSAVA
manual of raptors, pigeons and passerine birds. Quedgeley, Gloucester (England):
British Small Animal Veterinary Association; 2008. p. 311–9.
27. Madadgar O, Salehi TZ, Ghafari MM, et al. Study of an unusual paratyphoid epornitic
in canaries (Serinus canaria). Avian Pathol 2009;38(6):437– 41.
28. Piccirillo A, Mazzariol S, Caliari D, et al. Salmonella Typhimurium phage type DT160
infection in two Moluccan cockatoos (Cacatua moluccensis): clinical presentation
and pathology. Avian Dis 2010;54(1):131–5.
29. Gerlach H. Bacteria. In: Ritchie BW, Harrison GJ, Harrison LR, editors. Avian
medicine: principles and application. Lake Worth (FL): Wingers Publ., Inc.; 1994. p.
953– 6.
30. Harris JM. Zoonotic diseases of birds. Vet Clin North Am Small Anim Pract 1991;
21(6):1289 –98.
31. Madewell BR, McChesney AE. Salmonellosis in a human infant, a cat, and two
parakeets in the same household. J Am Vet Med Assoc 1975;167(12):1089 –90.
32. Morishita TY, Aye PP, Ley EC, et al. Survey of pathogens and blood parasites in
free-living passerines. Avian Dis 1999;43(3):549 –52.
33. Handeland K, Nesse LL, Lillehaug A, et al. Natural and experimental Salmonella
Typhimurium infections in foxes (Vulpes vulpes). Vet Microbiol 2008;132(1–2):
129 –34.
34. Joesph V. Infectious and parasitic diseases of captive passerines. Semin Avian
Exotic Pet Med 2003;12(1):21– 8.
35. Coburn B, Grassl GA, Finlay BB. Salmonella, the host and disease: a brief review.
Immunol Cell Biol 2007;85(2):112– 8.
36. Owens MD. Salmonella infection in emergency medicine. Available at: http://
emedicine.medscape.com/article/785774-print. Accessed February 10, 2011.
37. Centers for Disease Control and Prevention. Salmonella. Available at: http://www.
cdc.gov/salmonella/. Accessed February 10, 2011.
38. Ramesh N, Joseph SW, Carr LE, et al. Evaluation of chemical disinfectants for the
elimination of Salmonella biofilms from poultry transport containers. Poult Sci Jun
2002;81(6):904 –10.
39. Moretro T, Vestby LK, Nesse LL, et al. Evaluation of efficacy of disinfectants against
Salmonella from the feed industry. J Appl Microbiol 2009;106(3):1005–12.
40. Lennox AM. Mycobacteriosis in companion psittacine birds: a review. J Avian Med
Surg 2007;21(3):181–7.
41. Shitaye EJ, Grymova V, Grym M, et al. Mycobacterium avium subsp. hominissuis
infection in a pet parrot. Emerg Infect Dis 2009;15(4):617–9.
42. Campbell T. Mycobacterial tracheitis in a double-yellow-headed Amazon parrot
(Amazona ochrocephala oratrix). Exotic Pet Pract 1997;2(1):7.
43. AIDS Education & Training Centers National Resource Center Web site. Available at:
http://www.aidsetc.org/. Accessed February 10, 2011.
474 Evans

44. Centers for Disease Control and Prevention. You can prevent MAC (Disseminated
mycobacterium avium complex disease). Available at: http://www.cdc.gov/hiv/
resources/brochures/mac.htm. Accessed February 10, 2011.
45. Centers for Disease Control and Prevention. Tuberculosis (TB). Available at: http://
www.cdc.gov/tb/topic/basics/default.htm. Accessed February 10, 2011.
46. Steinmetz HW, Rutz C, Hoop RK, et al. Possible human-avian transmission of
Mycobacterium tuberculosis in a green-winged macaw (Ara chloroptera). Avian Dis
2006;50(4):641–5.
47. Schmidt V, Schneider S, Schlomer J, et al. Transmission of tuberculosis between
men and pet birds: a case report. Avian Pathol 2008;37(6):589 –92.
48. Hoop RK. Mycobacterium tuberculosis infection in a canary (Serinus canana) and a
blue-fronted Amazon parrot (Amazona amazona aestiva). Avian Dis 2002;46(2):
502– 4.
49. Tell LA, Foley J, Needham ML, et al. Diagnosis of avian mycobacteriosis: comparison
of culture, acid-fast stains, and polymerase chain reaction for the identification of
Mycobacterium avium in experimentally inoculated Japanese quail (Coturnix coturnix
japonica). Avian Dis 2003;47(2):444 –52.
50. Babcock S, Marsh AE, Lin J, et al. Legal implications of zoonoses for clinical
veterinarians. J Am Vet Med Assoc 2008;233(10):1556 – 62.
51. Best M, Sattar SA, Springthorpe VS, et al. Efficacies of selected disinfectants against
Mycobacterium tuberculosis. J Clin Microbiol 1990;28(10):2234 –39.
52. Bradbury JM, Morrow C. Avian mycoplasmas. In: Pattison M, McMullin PF, Bradbury
JM, editors. Poultry diseases. 6th edition. Edinburgh (Scotland): Saunders Elsevier;
2008. p. 220 –34.
53. Alexander DJ, Jones RC. Paramyxoviridae. In: Pattison M, McMullin PF, Bradbury
JM, editors. Poultry diseases. 6th edition. Edinburgh (Scotland): Saunders Elsevier;
2008. p. 294 –316.
54. Utterback WW, Schwartz JH. Epizootiology of velogenic viscerotropic Newcastle disease in
southern California, 1971–1973. J Am Vet Med Assoc 1973;163(9):1080–8.
55. Pearson GL, McCann MK. The role of indigenous wild, semidomestic, and exotic
birds in the epizootiology of velogenic viscerotropic Newcastle disease in southern
California, 1972–1973. J Am Vet Med Assoc 1975;167(7):610 – 4.
56. Senthuran S, Vijayarani K, Kumanan K, et al. Pathotyping of Newcastle disease virus
isolates from pet birds. Acta Virologica 2005;49(3):177– 82.
57. Mase M, Imada T, Sanada Y, et al. Imported parakeets harbor H9N2 influenza A
viruses that are genetically closely related to those transmitted to humans in Hong
Kong. J Virol 2001;75(7):3490 – 4.
58. Stanford M. Raptors: infectious diseases. In: Chitty J, Lierz M, editors. BSAVA
manual of raptors, pigeons and passerine birds. Quedgeley, Gloucester (England):
British Small Animal Veterinary Association; 2008. p. 212–22.
59. Jones MP. Selected infectious diseases of birds of prey. J Exot Pet Med 2006;15(1):
5–17.
60. Philippa J, Baas C, Beyer W, et al. Vaccination against highly pathogenic avian
influenza H5N1 virus in zoos using an adjuvanted inactivated H5N2 vaccine. Vaccine
2007;25(19):3800 – 8.
61. Hawkins MG, Crossley BM, Osofsky A, et al. Avian influenza A virus subtype H5N2
in a red-lored Amazon parrot. J Am Vet Med Assoc 2006;228(2):236 – 41.
62. U.S. Department of Agriculture, Animal and Plant Health Inspection Services. Protect
your pet from bird flu. Available at: http://www.aphis.usda.gov/publications/animal_
health/content/printable_version/ProtectYourPetBird2006.pdf. Accessed February
10, 2011.
 Zoonotic Diseases of Commonly Kept Pet Birds 475

63. West Nile virus infection in poultry. In: Kahn CM, Line S, Aiello SE, editors. The Merck
veterinary manual. 8th edition. Whitehouse Station (NJ): Merck & Co, Inc; 2008.
64. Pollock CG. West Nile virus in the Americas. J Avian Med Surg 2008;22(2):151–7.
65. Carboni DA, Nevarez JG, Tully TN, et al. West Nile Virus infection in a sun conure
(Aratinga solstitialis). J Avian Med Surg 2008;22(3):240 –5.
66. Sejvar JJ, Bode AV, Marfin AA, et al. West Nile virus-associated flaccid paralysis
outcome. Emerg Infect Dis 2006;12(3):514 – 6.
67. Centers for Disease Control and Prevention. West Nile Virus: what you need to know.
2006; Available at: http://www.cdc.gov/ncidod/dvbid/westnile/wnv_factsheet.htm.
Accessed February 10, 2011.
68. Mani I, Maguire JH. Small Animal zoonoses and immuncompromised pet owners.
Top Companion Anim Med 2009;24(4):164 –74.
69. Fenwick B, Takeshita K, Wong A. A moluccan cockatoo with disseminated crypto-
coccosis. J Am Vet Med Assoc 1985;187(11):1218 –9.
70. Lester SJ, Kowalewich NJ, Bartlett KH, et al. Clinicopathologic features of an
unusual outbreak of cryptococcosis in dogs, cats, ferrets, and a bird: 38 cases
(January to July 2003). J Am Vet Med Assoc 2004;225(11):1716 –22.
71. Abou-Gabal M, Atia M. Study of the role of pigeons in the dissemination of
Cryptococcus neoformans in nature. Sabouraudia 1978;16(1):63– 8.
72. Criseo G, Bolignano MS, Deleo F, et al. Evidence of canary droppings as as
important reservoir of Cryptococcus Neoformans. Int J Med Microbiol Virol Parasitol
Infect Dis 1995;282(3):244 –54.
73. Staib F, Schulz-Dieterich J. Cryptococcus neoformans in fecal matter of birds kept in
cages. Zentralbl Bakteriol Mikrobiol Hyg B 1984;179(2):179 – 86.
74. Raso TF, Werther K, Miranda E, et al. Cryptococcosis outbreak in psittacine birds in
Brazil. Med Mycol 2004;42(4):355– 62.
75. Rosario I, Acosta B, Colom F. Pigeons and other birds as a reservoir for Cryptococ-
cus spp. Revista Iberoamericana De Micologia 2008;25(1):S13– 8.
76. Terada T. Cryptococcosis in the central nervous system in a 36-year-old Japanese
man: an autopsy study. Tohoku J Exp Med 2010;222(1):33–7.
77. Nosanchuk JD, Shoham S, Fries BC, et al. Evidence of zoonotic transmission
Cryptococcus neoformans from a pet cockatoo to an immunocompromised patient.
Ann Intern Med 2000;132(3):205– 8.
78. Lagrou K, Van Eldere J, Keuleers S, et al. Zoonotic transmission of Cryptococcus
neoformans from a magpie to an immunocompetent patient. J Intern Med 2005;
257(4):385– 8.
79. Staib F. Sampling and isolation of Cryptococcus neoformans from indoor air with
the aid of the Reuter Centrifugal Sampler (RCS) and guizotia abyssinica creatinine
agar. A contribution to the mycological-epidemiological control of Cr. neofor-
mans in the fecal matter of caged birds. Zentralbl Bakteriol Mikrobiol Hyg B
1985;180(5– 6):567–75.
80. Rosen T, Jablon J. Infectious threats from exotic pets: dermatological implications.
Dermatol Clin 2003;21(2):229 –36.
81. Tsai SS, Hirai K, Itakura C. Histopathological survey of protozoa, helminths, and
ascardis of imported and local psittacine and passerine birds in Japan. Jpn J Vet Res
1992;40(4):161–74.
82. Gondim LSQ, Abe-Sandes K, Uzeda RS, et al. Toxoplasma gondii and Neospora
caninum in sparrows (Passer domesticus) in the Northeast of Brazil. Vet Parasitol
2010;168(1–2):121– 4.
83. Abreu-Acosta N, Foronda-Rodriguez P, Lopez M, et al. Occurrence of Cryptospo-
ridium hominis in pigeons (Columba livia). Acta Parasitologica 2009;54(1):1–5.
476 Evans

84. Kassa H, Harrington BJ, Bisesi MS. Cryptosporidiosis: a brief literature review and
update regarding Cryptosporidium in feces of Canada geese (Branta canadensis). J
Environ Health 2004;66(7):34 –9.
85. Majewska AC, Graczyk TK, Slodkowicz-Kowalsk A, et al. The role of free-ranging,
captive, and domestic birds of Western Poland in environmental contamination with
Cryptosporidium parvum oocysts and Giardia lamblia cysts. Parasitol Res 2009;
104(5):1093–9.
86. Plutzer J, Tomor B. The role of aquatic birds in the environmental dissemination of
human pathogenic Giardia duodenalis cysts and Cryptosporidium oocysts in Hun-
gary. Parasitol Int 2009;58(3):227–31.
87. Schets FA, van Wijnen JH, Schijven JF, et al. Monitoring of waterborne pathogens in
surface waters in Amsterdam, The Netherlands, and the potential health risk asso-
ciated with exposure to Cryptosporidium and Giardia in these waters. Appl Environ
Microbiol 2008;74(7):2069 –78.
88. Andrzejewska I, Tryjanowski P, Zduniak P, et al. Toxoplasma gondii antibodies in the
white stork (Ciconia ciconia). Berlin Munch Tierarztl Wochenschr 2004;117(7– 8):
274 –5.
89. Leite AS, Alves LC, Faustino MAG. Serological survey of toxoplasmosis in birds from
Cracidae family in a wild bird center facility at Pernambuco State, Northeast of Brazil.
Medicina Veterinaria-Recife 2007;1(1):55–7.
90. McDonnell PA, Scott KGE, Teoh DA, et al. Giardia duodenalis trophozoites isolated
from a parrot (Cacatua galerita) colonize the small intestinal tracts of domestic kittens
and lambs. Vet Parasitol 2003;111(1):31– 46.
91. Centers for Disease Control and Prevention. Parasites. Available at: http://www.cdc.
gov/parasites/. Accessed February 10, 2011.
92. Orton DI, Warren LJ, Wilkinson JD. Avian mite dermatitis. Clin Exp Dermatol
2000;25(2):129 –31.
93. Lacasse Y, Cormier Y. Hypersensitivity pneumonitis. Orphanet J Rare Dis 2006;1:25.
94. Tully TN Jr, Harrison GJ. Pneumonology. In: Ritchie BW, Harrison GJ, Harrison LR,
editors. Avian medicine: principles and application. Lake Worth (FL): Wingers Pub-
lishing, Inc; 1994. p. 556 – 81.
95. Phalen DN. Respiratory medicine of cage and aviary birds. Vet Clin North Am Exot
Anim Pract 2000;3(2):423–52.
96. Reavill DR. The differential diagnosis. Presented at the Association of Avian Veteri-
narians Conference. Providence (RI), August, 2007.
97. Hoppin JA, Umbach DM, Kullman GJ, et al. Pesticides and other agricultural factors
associated with self-reported farmer’s lung among farm residents in the Agricultural
Health Study. Occup Environ Med 2007;64(5):334 – 41.
98. Morell F, Roger A, Reyes L, et al. Bird fancier’s lung: a series of 86 patients. Medicine
(Baltimore) 2008;87(2):110 –30.
99. Caruana M, Cornish KS, Bajada S, et al. Rosella parrot exposure as a cause of bird
fancier’s lung. Arch Environ Occup H 2005;60(4):187–92.
100. Funke M, Fellrath JM. Hypersensitivity pneumonitis secondary to lovebirds: a new
cause of bird fancier’s disease. Eur Respir J 2008;32(2):517–21.
101. Gorman J, Cook A, Ferguson C, et al. Pet birds and risks of respiratory disease in
Australia: a review. Aust N Z J Public Health 2009;33(2):167–72.
102. Larson JM, Gerlach SY, Blair JE, et al. Mycobacterium chelonae/abscessus infec-
tion caused by a bird bite. Infect Dis Clin Pract 2008;16(1):60 –1.
103. Tripathi AK, Erdmann MWH. Bird-bite infection and pyoderma gangrenosum: a rare
combination? J Plast Reconstr Aesthetic Surg 2008;61(11):1409 –11.